scholarly journals Post-traumatic administration of the p53 inactivator pifithrin-α oxygen analogue reduces hippocampal neuronal loss and improves cognitive deficits after experimental traumatic brain injury

2016 ◽  
Vol 96 ◽  
pp. 216-226 ◽  
Author(s):  
Ling-Yu Yang ◽  
Nigel H. Greig ◽  
Ya-Ni Huang ◽  
Tsung-Hsun Hsieh ◽  
David Tweedie ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Deficits ◽  
Neuronal Loss ◽  
Post Traumatic ◽  
Experimental Traumatic Brain Injury

scholarly journals Pyruvate treatment attenuates cerebral metabolic depression and neuronal loss after experimental traumatic brain injury

2016 ◽  
Vol 1642 ◽  
pp. 270-277 ◽  
Author(s):  
Nobuhiro Moro ◽  
Sima S. Ghavim ◽  
Neil G. Harris ◽  
David A. Hovda ◽  
Richard L. Sutton
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuronal Loss ◽  
Metabolic Depression ◽  
Experimental Traumatic Brain Injury

scholarly journals Understanding neurodegeneration after traumatic brain injury: from mechanisms to clinical trials in dementia

2019 ◽  
Vol 90 (11) ◽  
pp. 1221-1233 ◽  
Author(s):  
Neil SN Graham ◽  
David J Sharp
Keyword(s):  
Traumatic Brain Injury ◽  
Clinical Trials ◽  
Brain Injury ◽  
Chronic Traumatic Encephalopathy ◽  
Diffuse Axonal Injury ◽  
Neuronal Loss ◽  
Long Term Effects ◽  
Neurofilament Light ◽  
Positron Emission ◽  
Post Traumatic

Traumatic brain injury (TBI) leads to increased rates of dementia, including Alzheimer’s disease. The mechanisms by which trauma can trigger neurodegeneration are increasingly understood. For example, diffuse axonal injury is implicated in disrupting microtubule function, providing the potential context for pathologies of tau and amyloid to develop. The neuropathology of post-traumatic dementias is increasingly well characterised, with recent work focusing on chronic traumatic encephalopathy (CTE). However, clinical diagnosis of post-traumatic dementia is problematic. It is often difficult to disentangle the direct effects of TBI from those produced by progressive neurodegeneration or other post-traumatic sequelae such as psychiatric impairment. CTE can only be confidently identified at postmortem and patients are often confused and anxious about the most likely cause of their post-traumatic problems. A new approach to the assessment of the long-term effects of TBI is needed. Accurate methods are available for the investigation of other neurodegenerative conditions. These should be systematically employed in TBI. MRI and positron emission tomography neuroimaging provide biomarkers of neurodegeneration which may be of particular use in the postinjury setting. Brain atrophy is a key measure of disease progression and can be used to accurately quantify neuronal loss. Fluid biomarkers such as neurofilament light can complement neuroimaging, representing sensitive potential methods to track neurodegenerative processes that develop after TBI. These biomarkers could characterise endophenotypes associated with distinct types of post-traumatic neurodegeneration. In addition, they might profitably be used in clinical trials of neuroprotective and disease-modifying treatments, improving trial design by providing precise and sensitive measures of neuronal loss.

scholarly journals Neuroprotective Effects of Geranylgeranylacetone in Experimental Traumatic Brain Injury

2013 ◽  
Vol 33 (12) ◽  
pp. 1897-1908 ◽  
Author(s):  
Zaorui Zhao ◽  
Alan I Faden ◽  
David J Loane ◽  
Marta M Lipinski ◽  
Boris Sabirzhanov ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Enhanced Recovery ◽  
Apoptotic Cell ◽  
Neuronal Loss ◽  
Lesion Size ◽  
Neuroprotective Effects ◽  
Stroke Models ◽  
Neuroprotective Actions ◽  
Experimental Traumatic Brain Injury

Geranylgeranylacetone (GGA) is an inducer of heat-shock protein 70 (HSP70) that has been used clinically for many years as an antiulcer treatment. It is centrally active after oral administration and is neuroprotective in experimental brain ischemia/stroke models. We examined the effects of single oral GGA before treatment (800 mg/kg, 48 hours before trauma) or after treatment (800 mg/kg, 3 hours after trauma) on long-term functional recovery and histologic outcomes after moderate-level controlled cortical impact, an experimental traumatic brain injury (TBI) model in mice. The GGA pretreatment increased the number of HSP70+ cells and attenuated posttraumatic α-fodrin cleavage, a marker of apoptotic cell death. It also improved sensorimotor performance on a beam walk task; enhanced recovery of cognitive/affective function in the Morris water maze, novel object recognition, and tail-suspension tests; and improved outcomes using a composite neuroscore. Furthermore, GGA pretreatment reduced the lesion size and neuronal loss in the hippocampus, cortex, and thalamus, and decreased microglial activation in the cortex when compared with vehicle-treated TBI controls. Notably, GGA was also effective in a posttreatment paradigm, showing significant improvements in sensorimotor function, and reducing cortical neuronal loss. Given these neuroprotective actions and considering its longstanding clinical use, GGA should be considered for the clinical treatment of TBI.

scholarly journals Computer-based cognitive stimulation for posttraumatic cognitive impairment: a clinical case

2020 ◽  
Vol 12 (6) ◽  
pp. 131-136
Author(s):  
E. M. Zubritskaya ◽  
S. V. Prokopenko ◽  
E. Yu. Mozheyko ◽  
V. A. Gurevich
Keyword(s):  
Traumatic Brain Injury ◽  
Cognitive Impairment ◽  
Brain Injury ◽  
Cognitive Deficits ◽  
Clinical Case ◽  
Positive Impact ◽  
Cognitive Stimulation ◽  
Moderate Cognitive Impairment ◽  
Computer Based ◽  
Post Traumatic

The paper describes a clinical case of applying a set of computer-based stimulation programs for cognitive impairment arising from severe open traumatic brain injury (TBI). It demonstrates the rehabilitation capabilities of a set of «Neurotechnology+» stimulation programs for correction of cognitive deficits in patients with dysregulated moderate cognitive impairment resulting from experienced severe open TBI. It is noted that the use of a set of the programs contributed to the improvement of impaired regulatory and neurodynamic functions, the expansion of phonemic and semantic speech activity, and the improvement of memory processes. The described case suggests that computer-based cognitive training has a positive impact on cognitive recovery after post-traumatic brain injury.

Cognitive Deficits Post-Traumatic Brain Injury and Their Association with Injury Severity and Gray Matter Volumes

2017 ◽  
Vol 34 (7) ◽  
pp. 1466-1472 ◽  
Author(s):  
Abigail Livny ◽  
Anat Biegon ◽  
Tammar Kushnir ◽  
Sagi Harnof ◽  
Chen Hoffmann ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Gray Matter ◽  
Cognitive Deficits ◽  
Injury Severity ◽  
Post Traumatic ◽  
Gray Matter Volumes

scholarly journals Increased Behavioral Deficits and Inflammation in a Mouse Model of Co-Morbid Traumatic Brain Injury and Post-Traumatic Stress Disorder

ASN NEURO ◽  
2020 ◽  
Vol 12 ◽  
pp. 175909142097956
Author(s):  
Arman Fesharaki-Zadeh ◽  
Jeremy T. Miyauchi ◽  
Karrah St. Laurent-Arriot ◽  
Stella E. Tsirka ◽  
Peter J. Bergold
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Deficits ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Barnes Maze ◽  
Post Traumatic Stress ◽  
Place Avoidance ◽  
Post Traumatic

Comorbid post-traumatic stress disorder with traumatic brain injury (TBI) produce more severe affective and cognitive deficits than PTSD or TBI alone. Both PTSD and TBI produce long-lasting neuroinflammation, which may be a key underlying mechanism of the deficits observed in co-morbid TBI/PTSD. We developed a model of co-morbid TBI/PTSD by combining the closed head (CHI) model of TBI with the chronic variable stress (CVS) model of PTSD and examined multiple behavioral and neuroinflammatory outcomes. Male C57/Bl6 mice received sham treatment, CHI, CVS, CHI then CVS (CHI → CVS) or CVS then CHI (CVS → CHI). The CVS → CHI group had deficits in Barnes maze or active place avoidance not seen in the other groups. The CVS → CHI, CVS and CHI → CVS groups displayed increased basal anxiety level, based on performance on elevated plus maze. The CVS → CHI had impaired performance on Barnes Maze, and Active Place Avoidance. These performance deficits were strongly correlated with increased hippocampal Iba-1 level an indication of activated MP/MG. These data suggest that greater cognitive deficits in the CVS → CHI group were due to increased inflammation. The increased deficits and neuroinflammation in the CVS → CHI group suggest that the order by which a subject experiences TBI and PTSD is a major determinant of the outcome of brain injury in co-morbid TBI/PTSD.

scholarly journals Cognitive retraining in traumatic brain injury

2012 ◽  
Author(s):  
Diya Nangia ◽  
Keshav Kumar
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Functioning ◽  
Cognitive Deficits ◽  
Single Case ◽  
Cognitive Impairments ◽  
Cognitive Retraining ◽  
The Family ◽  
History Of ◽  
Post Traumatic

Traumatic brain injury (TBI) is often associated with cognitive impairments. The psychological sequelae of cognitive deficits and emotional problems contribute significantly to the disability in the patient and to the distress of the family. The study aimed to develop a cognitive retraining programme to enhance cognitive functioning in TBI. 25 years old male presenting with history of left temporal hemorrhagic contusion with cerebral edema underwent 2 months of a cognitive retaining programme, addressing executive functions impairment. A single case experimental design with pre- and postassessment was adopted to evaluate changes in the patient in response to the intervention. Improvements were found in cognitive functioning, and in symptom reduction and behaviour. The 2 months hospital based cognitive retraining programme was found to be efficacious in ameliorating symptoms and improving cognitive, social and occupational functioning post traumatic brain injury.

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